Project description:Chitin, a polymer of N-acetyl-glucosamne, is a component of the cell walls of many plant fungal pathogens. During the infection process, the released chitin fragments (such as chitooctaose) from fungal cell walls by plant enzymes can trigger plant defense response and gene activation. The current work studies the regulation of Arabidopsis genes by the purified chitin fragment chitooctaose. We used the Affymetric Arabidopsis whole gene arrays to study the gene expression caused by chitin (chitooctaose). Keywords: chitooctaose vs water treatments, with 3 biological replicates
Project description:Chitin, a polymer of N-acetyl-glucosamne, is a component of the cell walls of many plant fungal pathogens. During the infection process, the released chitin fragments (such as chitooctaose) from fungal cell walls by plant enzymes can trigger plant defense response and gene activation. The current work studies the regulation of Arabidopsis genes by the purified chitin fragment chitooctaose. We used the Affymetric Arabidopsis whole gene arrays to study the gene expression caused by chitin (chitooctaose). Experiment Overall Design: Arabidopsis seedlings grown hydroponically for 14 days were treated with the purified chitin fragment chitooctaose at a final concentration of 1 um for 3 minutes. The controls were similarli treated with an equivalent amount of ddH2O. Three biological replicates were obtained.
Project description:Chitin oligomers, released from fungal cell walls by endochitinase, induce defense and related cellular responses in many plants. However, little is known about chitin responses in the model plant Arabidopsis. We describe here a large scale characterization of gene expression patterns in Arabidopsis in response to chitin treatment using an Arabidopsis microarray consisting of 2,375 EST clones representing putative defense-related and regulatory genes. Transcript levels for 71 ESTs, representing 61 genes, were altered >3-fold in chitin-treated seedlings relative to control seedlings. A number of transcripts exhibited altered accumulation as early as 10 min after exposure to chitin, representing some of the earliest changes in gene expression observed in chitin-treated plants. Included among the 61 genes are those that have been reported to be elicited by various pathogen-related stimuli in other plants. Additional genes, including genes of unknown function, were also identified broadening our understanding of chitin-elicited responses. Among transcripts with enhanced accumulation, one cluster was enriched in genes with both the W-box promoter element and a novel regulatory element. In addition, a number of transcripts had decreased abundance, encoding several proteins involved in cell wall strengthening and wall deposition. The chalcone synthase promoter element was identified in the upstream regions of these genes, suggesting that pathogen signals may suppress expression of some genes. These data indicate that Arabidopsis will be an excellent model to elucidate mechanisms of chitin elicitation in plant defense.
Project description:Microbes of the root-associated microbiome contribute to improve resilience and fitness of plants. In this study, the interaction between the salt stress tolerance-inducing beneficial bacterium Enterobacter sp. SA187 and Arabidopsis was investigated with a special focus on the plant immune system. Among the immune signalling mutants, the Lys-motif receptors LYK4 strongly affected the beneficial interaction. Overexpression of the chitin receptor components LYK4 compromised the beneficial effect of SA187 on Arabidopsis. Transcriptome analysis revealed that the role of LYK4 in immunity is intertwined with a function in remodeling defense responses. Overall, our data indicate that components of the plant immune system are key elements in mediating beneficial metabolite-induced plant abiotic stress tolerance.
Project description:A LysM Receptor-like Kinase Mediates Chitin Perception and Fungal Resistance in Arabidopsis Jinrong Wan,1 Xuecheng Zhang,1 David Neece,2 Katrina M. Ramonell,3 Steve Clough,2,4 Sung-yong Kim,1 Minviluz Stacey,1 and Gary Stacey1* 1Division of Plant Sciences, National Center for Soybean Biotechnology, C.S. Bond Life Sciences Center, University of Missouri-Columbia, Columbia, MO 65211, USA 2Department of Crop Sciences, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA 3Department of Biological Sciences, University of Alabama, Tuscaloosa, AL 35487, USA 4US Department of Agriculture, Soybean/Maize Germplasm, Pathology and Genetics Research, Urbana, IL 61801, USA *To whom correspondence should be addressed. E-mail: staceyg@missouri.edu Abstract: Chitin, a polymer of N-acetyl-D-glucosamine, is found in fungal cell walls, but not in plants. Plant cells are capable of perceiving chitin fragments (chitooligosaccharides) to trigger various defense responses. We identified a LysM receptor-like protein (AtLysM RLK1) that is required for the perception of chitooligosaccharides in Arabidopsis. Mutation of this gene blocked the induction of almost all chitooligosaccharide-responsive genes (CRGs) and led to more susceptibility to fungal pathogens, but not to a bacterial pathogen. In addition, exogenously applied chitooligosaccharides enhanced resistance against both fungal and bacterial pathogens in the wild-type plants, but not in the mutant. Together, our data strongly suggest AtLysM RLK1 is the chitin receptor or a key part of the receptor complex and chitin is a PAMP (pathogen-associated molecular pattern) in fungi recognized by the receptor leading to the induction of plant innate immunity against fungal pathogens. Since LysM RLKs were also recently shown to be critical for the perception of the rhizobial lipo-chitin Nod signals, our data suggest that LysM RLKs not just recognize friendly symbiotic rhizobia (via their lipo-chitin Nod signals), but also hostile fungal pathogens (via their cell wall chitin). These data suggest a possible evolutionary relationship between the perception mechanisms of Nod signals and chitin by plants. Keywords: chitooctaose, chitin receptor mutant